ArticleNature communications2016
Convulsive seizures from experimental focal cortical dysplasia occur independently of cell misplacement.
Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
What it found
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Who cites it
65 citing papers in PubMed, 117 citations in OpenAlex.
- Mild malformation of cortical development with oligodendroglial hyperplasia in epilepsy (MOGHE): genetics, mechanisms and precision therapy.Acta neuropathologica · 2026Review
- Focal cortical dysplasias: modeling pediatric drug-resistant epilepsy using human brain organoids.Frontiers in cellular neuroscience · 2026Review
- 4-Aminopyridine induced hyperpolarizing oscillations in pediatric human epileptic tissue are network-driven potassium currents that are abolished by activation of KCNQ2-5 (Kv7.2-Kv7.5) channels.Neurobiology of disease · 2026Article
- Seizure occurrence in FCD type II is predicted by lesion position and linked to cytoarchitectural alterations.Acta neuropathologica communications · 2025Article
- Ablation of dysmorphic neurons is a safe and effective treatment for focal cortical dysplasia II.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Cortical Dysplasia Beyond mTOR: Cellular Senescence Takes a Toll.Neuroscience bulletin · 2025Article
- Focal postnatal deletion ofFrontiers in molecular neuroscience · 2025Article
- Reducing Filamin A Restores Cortical Synaptic Connectivity and Early Social Communication Following Cellular Mosaicism in Autism Spectrum Disorder Pathways.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Focal cortical dysplasia (type II) detection with multi-modal MRI and a deep-learning framework.Npj imaging · 2024Article
- The molecular genetics of PI3K/PTEN/AKT/mTOR pathway in the malformations of cortical development.Genes & diseases · 2024Review
- Raising New Hope for Controlling Seizures in Focal Cortical Dysplasia with Gene Therapy.Neuroscience bulletin · 2024Article
- Targeting pathological cells with senolytic drugs reduces seizures in neurodevelopmental mTOR-related epilepsy.Nature neuroscience · 2024Article
- Extracellular glutamate and GABA transients at the transition from interictal spiking to seizures.Brain : a journal of neurology · 2024Article
- The mTOR pathway geneseLife · 2024Article
- Phenotypic and genotypic characterization of NPRL3-related epilepsy: Two case reports and literature review.Epilepsia open · 2024Review
- Gene therapy for seizures in focal cortical dysplasia.Nature reviews. Neurology · 2024Article
- Anti-seizure gene therapy for focal cortical dysplasia.Brain : a journal of neurology · 2024Article
- The mTOR pathway genesbioRxiv : the preprint server for biology · 2024Article
- Between neurons and networks: investigating mesoscale brain connectivity in neurological and psychiatric disorders.Frontiers in neuroscience · 2024Review
- Potential roles of voltage-gated ion channel disruption in Tuberous Sclerosis Complex.Frontiers in molecular neuroscience · 2024Article
5 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Focal cortical dysplasia (FCD), a local malformation of cortical development, is the most common cause of pharmacoresistant epilepsy associated with life-long neurocognitive impairments. It remains unclear whether neuronal misplacement is required for seizure activity. Here we show that dyslamination and white matter heterotopia are not necessary for seizure generation in a murine model of type II FCDs. These experimental FCDs generated by increasing mTOR activity in layer 2/3 neurons of the medial prefrontal cortex are associated with tonic-clonic seizures and a normal survival rate. Preventing all FCD-related defects, including neuronal misplacement and dysmorphogenesis, with rapamycin treatments from birth eliminates seizures, but seizures recur after rapamycin withdrawal. In addition, bypassing neuronal misplacement and heterotopia using inducible vectors do not prevent seizure occurrence. Collectively, data obtained using our new experimental FCD-associated epilepsy suggest that life-long treatment to reduce neuronal dysmorphogenesis is required to suppress seizures in individuals with FCD.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.